Stroke scientists gather more evidence for presence of ‘gut-brain axis’
Research on mice by scientists at The University of Manchester has shed new light on why the guts’ immune system changes after a stroke and how it might contribute to gastro-intestinal problems.
Published in Brain, Behaviour and Immunity, the study adds to the emerging idea of the “gut-brain axis” – in which scientists suggest allows communication between the two organs in both health and disease.
The study casts more light on the biology of stroke, a life-threatening medical emergency that disrupts blood flow to parts of the brain often causing long-term effects to mobility and cognition.
Stroke patients are also at risk of secondary bacterial infections and often exhibit gastrointestinal symptoms including difficulty swallowing and constipation.
Increasing evidence suggests these gastrointestinal complications are associated with changes in the commensal microbiota – the community of “good bacteria” that normally keep our guts healthy.
The changes are seen both in stroke patients and in animal models of stroke, yet the underlying reasons for these gut symptoms and their importance for stroke severity or recovery have been poorly understood.
Previous studies from scientists who co-authored the current study have shown how signals from the nervous system may act to change gut immune responses following stroke.
The latest study, funded by the Wellcome Trust, shows the axis may also work in both directions, with antibody-producing immune cells moving to the brain and the associated membranes during stroke – although the importance of this for stroke severity and prognosis is not yet known.
Using mice, the team studied the changes that happened in the small intestine after a stroke, revealing populations of immune cells that make antibodies became altered in the first few days.
In particular they found that a specialised subset of cells that make an antibody called Immunoglobulin A (IgA) became hyper-activated. IgA acts to manage the populations of commensal bacteria that live in the intestine and determine gut health.
The researchers then found that mice lacking IgA do not exhibit the same degree of changes to the gut microbiome following stroke – suggesting altered immune function could in part explain some changes seen in the intestinal tract of stroke patients.
Working with neuroscientists, we were able to begin to uncover how the immune system in the gut becomes disturbed following a stroke, and how that might lead to changes in the way the gut deals with its “good bacteria”
Lead investigator Professor Matt Hepworth from the Lydia Becker Institute of Immunity and Inflammation at The University of Manchester said: “Stroke is a devastating neurological event but also has many long-term consequences that can leave the patient at risk of airway infection, as well as gastrointestinal complications.
“Working with neuroscientists, we were able to begin to uncover how the immune system in the gut becomes disturbed following a stroke, and how that might lead to changes in the way the gut deals with its “good bacteria”.
“We now think these immune changes might contribute to the intestinal symptoms and long-term complications seen in stroke patients.”
He added: “While the focus remains on stroke prevention, as well as early intervention to minimise the damage in patients who do suffer stroke we reveal new understanding of the secondary pathologies experienced throughout the body and that contribute to long-term complications for recovering patients.
“As immune-targeting therapeutics are increasingly used in the clinic, this opens up the possibility of treating immune driven disease symptoms following a stroke to improve patients’ quality of life.”
- The paper Cerebral ischaemic stroke results in altered mucosal antibody responses and host-commensal microbiota interactions available . DOI: 10.1016/j.bbi.2025.106184.